Echinococcus spp. are zoonotic cestode parasites responsible for cystic Echinococcosis (CE), one of the designated neglected tropical diseases by the World Health Organization [1]. The parasite cycles between intermediate ungulate hosts and canid definitive hosts as hydatid cysts in various organs and adult worms in the small intestines, respectively. Humans become incidentally infected with the parasite following ingestion of infective eggs shed in the feces of definitive canid hosts. The resulting pulmonary and hepatic cysts, termed hydatid cysts, are difficult to diagnose and treat in intermediate animal hosts and aberrant human hosts, cause substantial economic loss, and can be fatal as cysts compress host tissues or rupture within the host [2].
There are currently 10 recognized genotypes (G1-G10) which correspond to distinct species within the Echinococcus granulosus sensu lato (s.l.) complex. Each species differs in its host specificity, phenotypic and genetic characteristics, and pathogenicity patterns. The E. . granulosus sensu stricto complex (G1-G3) includes the sheep strain, the Tasmanian sheep strain, and the buffalo strain, respectively and typically involves domestic livestock and domestic canines in its lifecycle. E. equinus (G4) is the horse stain and is specific to equids and E. ortleppi (G5) is the cattle strain, and typically cycles between cattle and dogs. E. intermedius (G6-G7), which are grouped with E. canadensis under some classification schemes, includes the camel and pig strains. E. canadensis (G8-G10) encompasses the American cervid strain and the Fennoscandian cervid strain, and cycles between cervids including moose, elk, and reindeer and canids. [4, 5, 6]. Members of E. granulosus sensu stricto are most frequently implicated as the causative agents of CE; however, E. ortleppi (G5), E. intermedius (G6-7), and E. canadensis (G8, G10) are also known contribute to the global burden of human disease [4,7,8].
In 2000, the Tennessee Wildlife Resources Agency (TWRA) implemented a re-establishment plan for elk (Cervus canadensis) into the Sundquist Wildlife Management and Royal Blue Wildlife Management Area (WMA) public lands in Campbell, Scott, Morgan, Claiborne, and Anderson Counties of Tennessee [9,10,11]. Royal Blue WMA has since been absorbed into the North Cumberland Wildlife Management Area (NCWMA). Additionally, in 2001, the National Parks Service reintroduced elk into the Cataloochee Valley area of the Great Smoky Mountains National Park (GSMNP). In both locations, elk had been extirpated since the mid-1800s [12]. From 2000 to 2008, a total of 201 elk were released into the NCWMA, and from 2001 to 2002, 52 elk were released into the GSMNP [9,10,13]. A 2016 TWRA survey documented 349 elk within NCWMA, suggesting that the reintroduction was successful to date, and populations have remained steady in subsequent years [13]. In both locations, re-introduced elk were originally sourced from Elk Island National Park (EINP) in Alberta, Canada due to the park’s history of disease testing animals and having the Manitoban subspecies (C. c. manitobensis), which is considered the closest genetic stock to the extinct eastern elk (C. c. canadensis). A portion of the imported elk came from Land Between the Lakes (LBL) National Recreation Area, Kentucky; however, all LBL elk were originally sourced from EINP. Prior to translocation, elk were screened for major pathogens, including brucellosis, bovine tuberculosis, Johne’s disease, anaplasmosis, vesicular stomatitis, bluetongue, epizootic hemorrhagic disease, infectious bovine rhinotracheitis/bovine viral diarrhea, and several strains of leptospirosis [10]. However, antemortem testing for Echinococcus was not available.Echinococcus granulosus s.l. is not currently considered endemic in GSMNP or NCWMA, but since the reintroduction of elk, the E. granulosus s.l. strain G10 (i.e. E. canadensis) has been presumptively diagnosed in one elk at necropsy. Moreover, an E. granulosus s.l. infection has been suspected in several other elk [14]. No previous reports of echinococcosis in wildlife in this region exist, although they are well documented in wildlife in Canada [15,16].
With the reintroduction of elk into the NCWMA and GSMNP ecosystems, a pathway for the maturation and spread of Echinococcus was newly recreated. It is an emerging concern that the transmission of Echinococcus from the translocated animals into wild or domestic canine populations and other sympatric cervids has occurred, thereby establishing a sustainable transmission cycle and reservoir for the disease. This creates a public health risk, as the GSMNP hosted 12.5 million recreational visitors in 2019 [17]. Similarly, NCWMA is a multi-purpose public land that hosts large numbers of visitors and issues 15 elk harvest permits annually [18]. Due to the high tourist load in these recreational areas and the presence of wild canids (coyotes, foxes) and free-roaming domestic dogs, both of which can serve as definitive hosts, there is increased opportunity for wildlife and domestic animal contact, as well as zoonotic transmission [19].
This study describes E. granulosus s.l. lesions and molecular characterization from necropsied elk from NCWMA and GSMNP and investigates parasite transmission in the NCWMA by examining coyote intestinal samples for eggs or protoscoleces. The establishment of a baseline prevalence and ecology data of this pathogen will help fill a critical void in the current awareness of the parasite. Due to the zoonotic potential of this pathogen, this information is vital to informing wildlife management policy, clinical medical and veterinary medical practice, and public health efforts [20].